Renal 8 Flashcards

1
Q

Give the names of the two main body fluid compartments and the percentage of total body water in each. Give the names of the two main subdivisions of the ECF and the percentage of the ECF in each division.

A
  • Intracellular fluid (2/3 of total body water)
    • Extracellular fluid (1/3 of total body water)
      • Interstitial fluid (75% of ECF)
      • Plasma (25% of ECF)
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2
Q

Compare the compositions of the ICF, with the ECF. (What are the main cations and anions for each?) State the main difference between the interstitial fluid and the intravascular portion (plasma) of the extracellular fluid compartment. (Why do they differ?)

A
  • ICF: cations  K+; anions  phosphate and proteins
    • ECF: cations  Na+; anions  Cl-, bicarbonate anion
      • Plasma has more proteins than interstitial fluid, but still more proteins in ICF
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3
Q

Explain why the ICF (intracellular fluid) is nearly always identical to the ECF (extracellular fluid) in osmotic concentration. How does the size and osmolality of the ICF and ECF compartments change with the ingestion of pure water? With the addition of isotonic saline? With the addition of hypertonic saline?

A

Water can move across the membrane and essentially dilute the osmoles equally on both sides of the membrane

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4
Q
  1. Explain what is meant by the term “ineffective osmole”. 5. Explain why elevated plasma urea concentrations do not elicit ADH release.
A
  • Na is an effective osmole
  • Ineffective: when the solute (osmole) can readily cross cell membranes it would not cause an osmorecptor to shrink nor would it cause net osmosis of water. Urea is permeable to the membrane so it is an ineffective osmole. A raised urea concentration would not elicit ADH release (this is because ADH is released when osmoreceptors shrink – which would not happen with urea because urea is freely permeable)
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5
Q

Explain how plasma osmolality and baroreceptor signals control the release of ADH.

A
  • Release of ADH from posterior pituitary is increased by an increase in osmolarity which causes shrinkage of the hypothalmic osmoreceptors. Osmolality plays a larger role than baroreceptors on ADH secretion until
  • ECF volume sensors indirectly sense intravascular pressure by assessing stretch in low pressure areas (cardiac atria/pulmonary vasc) and high pressure areas (carotid sinus/aortic arch). Low BP stimulates the release of ADH
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6
Q

Explain how plasma osmolality and baroreceptor signals affect thirst. How does angiotensin II affect thirst?

A
  • Thirst is also cause by shrinkage of thirst osmoreceptors in response to increased osmolality of ECF. Angiotensin II also acts on the brain to increase thirst via subfornical organ.
    • A large reduction in blood volume also stimulates thirst thru barorecptors.
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7
Q

Describe the alterations in blood pressure, sympathetic tone, renin secretion, angiotensin II production, and atrial natriuretic peptide production that occur when excess NaCl ingestion occurs in a salt sensitive individual.

A
  • Normal people can excrete a Na load without having an elevation of BP by suppressing renin secretion, increasing atrial natriuretic peptide
  • An increase in Na in ECF (possibly by action of Na/K ATPase pump) would increase blood pressure by increasing water in ECF (thru ADH, etc)
    • This would decrease the activity of sympathetic tone and decrease renin secretion  less angiotensin II and all its effects.
  • Plasma volume expansion stretches atria which increases release of ANP  inhibits renin, angiotensin II and Na reabsorption
  • Overall, effect of excessive salt ingestion is TEMPORARY EXPANSION OF ECF
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8
Q

Describe the body’s response to a sudden decrease in plasma/blood volume as the result of a hemorrhage.

A

Normal regulation of ADH secretion is mainly under control of plasma osmolality. The baroreceptor signals do not play a large effect on ADH secretion until blood loss is about 10%, then ADH secretion increases rapidly as blood loss increases above this level.

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9
Q

Briefly describe three effects of ADH on the kidney.

A
  • ADH binds vasopressin type 2 receptors on collecting duct and causes insertion of aquaporins into luminal aspect
  • Vasoconstricts pericytes around descending vasa recta  decreasing flow thru vasa recta (helps preserve medullary gradient needed to produce concentrated urine
  • Increases permeability of medullary collecting ducts to urea by increasing urea uniporters
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